Ask about this productRelated genes to: HOXA9 Blocking Peptide
- Gene:
- HOXA9 NIH gene
- Name:
- homeobox A9
- Previous symbol:
- HOX1G, HOX1
- Synonyms:
- -
- Chromosome:
- 7p15.2
- Locus Type:
- gene with protein product
- Date approved:
- 1990-06-15
- Date modifiied:
- 2014-11-18
Related products to: HOXA9 Blocking Peptide
Related articles to: HOXA9 Blocking Peptide
- Chronic non-bacterial osteomyelitis (CNO) is a rare autoinflammatory bone disease primarily affecting children and adolescents. Reliable biomarkers for diagnosis, disease monitoring, and prediction of disease course are lacking. This study demonstrates that, when compared to healthy participants, the proportion of 'pro-inflammatory' CD14CD16 'classical' monocytes is elevated in patients with CNO, before and after the initiation of treatment. Differential DNA methylation (200 hyper-, 162 hypo-methylated) profiles in monocytes from CNO patients affect key genes involved in immune regulation, including RUNX3, HOXA9, HLA-DMB, HLAB, MAP3K6, RXRB, CD163L1, MAP2, CDK6, HLA-G, HDAC10, and HLA-DQA1 genes. Notably, DNA methylation changes persist and potentially progress over time after the initiation of treatment with naproxen. In conclusion, patients with CNO display higher proportions of 'classical' monocytes when compared to healthy participants in conjunction with dysregulated DNA methylation patterns. Molecular alterations remain despite symptom relief with naproxen, suggesting progressive inflammation-mediated changes. - Source: PubMed
Publication date: 2026/05/15
Carlsson EmilGodoy-Tena GerardMorbach HennerGirschick Hermann JDissanayake DilanCharras AmandineBallestar EstebanHedrich Christian M - Benzene is a well-established environmental leukemogen, but how benzene-induced myelosuppression evolves into rapid malignant transformation remains unclear. To deconstruct this progression, Mll-Af9 chimeric mice were subjected to chronic benzene inhalation. Following exposure, mice exhibited prolonged hematotoxicity, but the initially suppressed white blood cells and CD45.2⁺ pre-leukemic cells progressively rebounded, significantly exceeding control levels by week 10. Serial colony-forming assays revealed suppressed clonogenic capacity at week 8, followed by a robust enhancement at week 10 that was predominantly driven by sustained colony-forming unit-granulocyte-macrophage progenitor (CFU-GM) expansion. These phenotypic shifts pinpointed the 8-10-week interval as the critical tipping point for the suppression-to-proliferation switch. Single-cell RNA sequencing identified granulocyte-macrophage progenitors (GMPs) as the principal cellular drivers of this transformation. During the suppressive phase, a distinct GMP subset displayed cell cycle arrest yet aberrantly co-activated myeloid differentiation (CEBPA) and pro-leukemic self-renewal (HOXA9/MEIS1) programs, accompanied by marked S100a8/S100a9 upregulation. This stress-adapted phenotype transcriptional state was associated with subsequent transcriptional reversal and clonal outgrowth that ultimately shortened overall survival. Clinical relevance was further supported by The Cancer Genome Atlas cohort, where elevated S100A8/S100A9 expression correlated with poorer survival in acute myeloid leukemia patients. Collectively, these findings delineate a stress-driven evolutionary pathway linking benzene-induced marrow suppression to early pre-leukemic adaptation and highlight S100a8/S100a9-associated transcriptional programs as potential early molecular features of benzene-related leukemogenic progression. - Source: PubMed
Publication date: 2026/05/12
Zhou JinSui PinpinLi YingHe JinxuLu YedanZheng MinSong XiangrongYu TaoCheng XiurongXing Caihong - Histone lysine methylation is a post-translational modification system that has a profound impact on gene expression. The methylation of H3K79 plays an important role in gene transcription, repair of DNA damage, and cell cycle. In recent years, it has been discovered that Disruptor of telomeric silencing 1-like (DOT1L) can methylate H3K79 and is the only known H3K79 methyltransferase. DOT1L activity in leukemia cells interacts with ubiquitinated H2B to promote nucleosome binding. AF family proteins bind DNA to ENL to recruit DOT1L to the promoters of KMT2A (formerly MLL1)-rearranged leukemia target genes, promoting HOXA9 overexpression, a key event in leukemia. Moreover, DOT1L O-GlcNAcylation promotes its protein stability and proliferation of MLL fusion leukemia cells. This review summarizes the structure, biological functions and upstream regulatory mechanisms of DOT1L-mediated H3K79 methylation. Relevant literature was searched in PubMed and Web of Science for studies published from 2000 to 2024 using keywords including "DOT1L," "H3K79 methylation" and "KMT2A leukemia." - Source: PubMed
Publication date: 2026/05/04
Chen ChuWu DiLv CanranZhu PengChen ZihaoLi QiLi JunmingYang JianZhang Jing - The HOXA gene locus coordinates body patterning, hematopoiesis, and differentiation. While studying blood phenotype-associated variation within the HOXA locus, we identified a genetic variant, rs17437411, associated with globally reduced blood counts, protection from blood cancers, and variation in anthropometric phenotypes. We found that this variant disrupts the activity of a previously unstudied antisense long non-coding RNA (lncRNA) located between HOXA7 and HOXA9, which we named HOXA opposite-strand transcript, stem-cell regulator, antisense mid-cluster between loci (HOTSCRAMBL). The HOTSCRAMBL variant disrupts lncRNA function and reduces human hematopoietic stem cell (HSC) self-renewal. Mechanistically, HOTSCRAMBL enables appropriate expression and splicing of HOXA genes in HSCs, most notably HOXA9, in an SRSF2-dependent manner. Given the critical role of HOXA gene expression in some blood cancers, we also demonstrate that HOTSCRAMBL variation or deletion compromises HOXA-dependent acute myeloid leukemias. Collectively, we show how insights from human genetic variation can uncover critical regulatory processes required for effective developmental gene expression. - Source: PubMed
Publication date: 2026/05/01
Lyu PengAgarwal GauravGuo Chun-JieSychla AdamBourgeois WallaceYe TianyiWeng ChenAntoszewski MateuszJoubran SamanthaCaulier AlexisPoeschla MichaelArmstrong Scott ARouskin SilviSankaran Vijay G - Chronic myeloid leukemia (CML) is a hematologic malignancy originating from hematopoietic stem cells with the fusion oncogene BCR-ABL1 on the Philadelphia chromosome, which drives the abnormal proliferation of leukemic blast cells within the bone marrow microenvironment. While previous research has primarily focused on the hematopoietic compartment, the functional contribution of the bone marrow microenvironment to the CML pathology remains understudied. We investigated the changes in the peripheral nervous system in the bone marrow with myeloid leukemia via immunofluorescence staining of tyrosine hydroxylase (TH) and calcitonin gene-related peptide (CGRP) antibodies in mouse with NUP98-HOXA9- and BCR-ABL1-expressing myeloid leukemia. We found that the TH-positive fibers were significantly reduced, while no overt changes were observed in CGRP-positive nerves in the bone marrow. The reduction in TH-positive nerve cells was also evident in the spleen. Human patient gene expression data suggested that the levels of sympathetic nerve receptor expression change during the blastic transformation of human CML. Our findings indicate that the sympathetic nervous system regulates the pathogenesis of myeloid leukemia and could play a crucial role in the disease progression of myeloid leukemia. - Source: PubMed
Publication date: 2026/04/13
Okigawa SayumiInafuku HibikiHattori AyunaIto Takahiro